Inactivation of GABA sub(A) receptor reduces ginsenoside Rb sub(3) neuroprotection in mouse hippocampal slices after oxygen-glucose deprivation

Aim of the study: To investigate the effect of ginsenoside Rb sub(3) on synaptic transmission after oxygen-glucose deprivation in vitro. Materials and methods: The population spike (PS) was recorded in the stratum pyramidale of mouse hippocampal slices using extracellular recordings. Results: Ginsen...

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Veröffentlicht in:Journal of ethnopharmacology 2011-01, Vol.133 (2), p.914-916
Hauptverfasser: Jiang, Shan, Miao, Bei, Song, Xuejun, Jiang, Zhenglin
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creator Jiang, Shan
Miao, Bei
Song, Xuejun
Jiang, Zhenglin
description Aim of the study: To investigate the effect of ginsenoside Rb sub(3) on synaptic transmission after oxygen-glucose deprivation in vitro. Materials and methods: The population spike (PS) was recorded in the stratum pyramidale of mouse hippocampal slices using extracellular recordings. Results: Ginsenoside Rb sub(3) depressed the basal synaptic transmission, which also promoted the recovery amplitude of PS after OGD in a concentration-dependent manner. The GABA sub(A) receptor agonist muscimol improved the recovery, which was similar to that of ginsenoside Rb sub(3). Moreover, the effect of ginsenoside Rb sub(3) in combination with muscimol was not additive. Treatment with the GABA sub(A) receptor antagonist bicuculline or picrotoxin, which prevented the depression of PS caused by ginsenoside Rb sub(3), also reduced the neuroprotection. Conclusion: The results indicate that the activation of the GABA sub(A) receptor is correlated with the neuroprotective mechanisms of ginsenoside Rb sub(3).
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source ScienceDirect Journals (5 years ago - present)
subjects Bicuculline
Brain slice preparation
Depression
Firing pattern
gamma -Aminobutyric acid A receptors
ginsenosides
Glucose
Muscimol
Neuroprotection
Oxygen
picrotoxin
Synaptic transmission
title Inactivation of GABA sub(A) receptor reduces ginsenoside Rb sub(3) neuroprotection in mouse hippocampal slices after oxygen-glucose deprivation
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